Feline Leukaemia Virus


Feline leukaemia virus (FeLV) is a gammaretrovirus that causes a variety of fatal diseases including leukaemia and lymphoma in its host, the domestic cat, and occasionally in large cat species. Many cats become persistently infected and develop disease after an incubation period of several years, during which virus can be transmitted to other cats. Disease is often associated with the generation of FeLV variants with increased pathogenic potential that can arise by mutation of envelope sequences, duplication of transcriptional enhancer elements or recombination with host proto‐oncogene sequences. FeLV can also produce variants by recombination with endogenous proviruses related to FeLV that are found in the domestic cat and its close relatives. The prevalence of FeLV infection has been reduced in many cat populations by isolation of infected carriers and more recently by vaccines that augment the natural ability of most cats to control infection.

Key Concepts:

  • The outcome of infection by FeLV depends on the infectious dose, age and immunocompetence of the host. Many cats achieve lifelong control, if not elimination of infection.

  • Cats that become persistently viraemic are at risk of a variety of FeLV‐related diseases after a latent period of up to several years.

  • The common infectious form, FeLV‐A can acquire altered entry receptor specificity by envelope gene mutation (to FeLV‐C) or recombination with endogenous FeLV‐related proviruses (to FeLV‐B).

  • FeLV envelope variants may induce fatal diseases of rapid onset including nonregenerative anaemia (FeLV‐C) or wasting and immunodeficiency (FeLV‐T).

  • The oncogenic potential of FeLV can evolve by duplication of transcriptional enhancer control elements in the long‐terminal repeat or by transduction of host proto‐oncogene sequences.

  • Although the immune parameters of vaccine protection remain unclear, FeLV demonstrates the feasibility of effective immunisation against the gamma retroviruses.

  • Commercial FeLV vaccines in recent or current use include inactivated FeLV, infected cell extracts, recombinant envelope protein and live recombinant poxvirus vaccines.

Keywords: retrovirus; FeLV; oncogene; transduction; endogenous retrovirus; receptor; transporter; leukaemia; lymphoma; immunodeficiency

Figure 1.

The natural history and epidemiology of infection with FeLV and its variants. The common infectious form of FeLV (FeLV‐A) is conserved in antigenic structure and of low pathogenicity. Most exposed cats control initial infection, whereas those that become persistently viraemic are at risk of developing fatal disease that may be associated with the evolution of a variant FeLV as shown (see Figure ). Contact transmission studies have shown that variants are not efficiently transmitted by natural spread.

Figure 2.

Origin and molecular structure of FeLV variants. FeLV‐B, C and T are envelope variants generated by mutations (C, T) or recombination with endogenous FeLV (B). FeLV‐onc are generated by recombination with cellular proto‐oncogene sequences (e.g. Myc, Abl, Fes, Fms and Kit), whereas FeLV‐LTRen+ are generated by duplication of enhancer sequences in the long‐terminal repeats.



Brown MA, Cunningham MW, Roca AL et al. (2008) Genetic characterization of feline leukemia virus from Florida panthers. Emerging Infectious Diseases 14: 252–259.

Cheng HH, Anderson MM, Hankenson FC et al. (2006) Envelope determinants for dual‐receptor specificity in feline leukemia virus subgroup A and T variants. Journal ofVirology 80: 1619–1628.

Flynn JN, Dunham SP, Watson V and Jarrett O (2002) Longitudinal analysis of feline leukemia virus‐specific cytotoxic T lymphocytes: correlation with recovery from infection. Journal of Virology 76: 2306–2315.

Fulton R, Plumb M, Shield L and Neil JC (1990) Structural diversity and nuclear protein binding sites in the long terminal repeats of feline leukaemia virus. Journal of Virology 64: 1675–1682.

Hardy WD Jr, McClelland AJ, Zuckermann EE et al. (1976) Prevention of contagious spread of FeLV and the development of leukaemia in pet cats. Nature 263: 326–328.

Hardy WD Jr, McClelland AJ, Zuckerman EE et al. (1980) Development of virus non‐producer lymphosarcomas in pet cats exposed to FeLV. Nature 288: 90–92.

Hoover EA, Olsen RG, Hardy WD Jr, Schaller JP and Mathes LE (1976) Feline leukemia virus infection: age‐related variation in response of cats to experimental infection. Journal of the National Cancer Institute 57: 365–369.

Jarrett O (1994) Feline leukaemia virus. In: Chandler EA, Gaskell CJ and Gaskell RM (eds) Feline Medicine and Therapeutics, 2nd edn, pp. 473–478. Oxford: Blackwell Scientific.

Jarrett O, Hardy WD Jr, Golder MC and Hay D (1978) The frequency of occurrence of feline leukaemia virus subgroups in cats. International Journal of Cancer 21: 334–337.

Jarrett WFH, Crawford E, Martin WB and Davie F (1964) Leukemia in the cat. A virus‐like particle associated with leukemia (lymphosarcoma). Nature 202: 567.

Major A, Cattori V, Boenzli E et al. (2010) Exposure of cats to low doses of FeLV: seroconversion as the sole parameter of infection. Veterinary Research 41: 17.

Matsumoto Y, Momoi Y, Watari T et al. (1992) Detection of enhancer repeats in the long terminal repeats of feline leukemia viruses from cats with spontaneous neoplastic and nonneoplastic diseases. Virology 189: 745–749.

McDougall A, Terry A, Tzavaras T et al. (1994) Defective endogenous viruses are expressed in feline lymphoid cells: evidence for a role in natural resistance to subgroup B feline leukemia viruses. Journal of Virology 68: 2151–2160.

Meli ML, Cattori V, Martinez F et al. (2010) Feline leukemia virus infection: a threat for the survival of the critically endangered Iberian lynx (Lynx pardinus). Veterinary Immunology and Immunopathology 134: 61–67.

Mendoza R, Anderson MM and Overbaugh J (2006) A putative thiamine transport protein is a receptor for feline leukemia virus subgroup A. Journal of Virology 80: 3378–3385.

Neil JC, Fulton R, Rigby M and Stewart M (1991) Feline leukaemia virus: generation of pathogenic and oncogenic variants. Current Topics in Microbiology and Immunology 171: 68–93.

Nunberg JH, Rogers G, Gilbert JH and Snead RM (1984) Method to map antigenic determinants recognized by monoclonal antibodies: localization of a determinant of virus neutralization on the feline leukemia virus envelope protein gp70. Proceedings of the National Academy of Sciences of the USA 81: 3675–3679.

Onions D, Jarrett O, Testa N, Frassoni N and Toth S (1982) Selective effect of feline leukaemia virus on early erythroid precursors. Nature 296: 156–158.

Prabhu S, Lobelle‐Rich PA and Levy LS (1999) The FeLV‐945 LTR confers a replicative advantage dependent on the presence of a tandem triplication. Virology 263: 460–470.

Quigley JG, Yang Z, Worthington MT et al. (2004) Identification of a human heme exporter that is essential for erythropoiesis. Cell 118: 757–766.

Ramsey IK, Spibey N and Jarrett O (1998) The receptor binding site of feline leukemia virus surface glycoprotein is distinct from the site involved in virus neutralization. Journal of Virology 72: 3268–3277.

Rigby MA, Rojko JL, Stewart MA et al. (1994) Partial dissociation of subgroup C phenotype and in vivo behaviour in feline leukaemia viruses with chimeric envelope genes. Journal of Virology 68: 8296–8303.

Rojko JL, Hoover EA, Mathes LE, Olsen RG and Schaller JP (1979) Pathogenesis of experimental feline leukemia virus infection. Journal of the National Cancer Institute 63: 59–68.

Russell PH and Jarrett O (1978) The specificity of neutralizing antibodies to feline leukaemia viruses. International Journal of Cancer 21: 768–778.

Shalev Z, Duffy SP, Adema K et al. (2009) Identification of a feline leukemia virus variant that can use THTR1, FLVCR1, and FLVCR2 for infection. Journal of Virology 83: 6706–6716.

Sparkes AH (1997) Feline leukaemia virus: a review of immunity and vaccination. Journal of Small Animal Practice 38: 187–194.

Stewart MA, Warnock M, Wheeler A et al. (1986) Nucleotide sequences of a feline leukemia virus subgroup A envelope gene and long terminal repeat and evidence for the recombinational origin of subgroup B viruses. Journal of Virology 58: 825–834.

Stützer B, Simon K, Lutz H et al. (2011) Incidence of persistent viraemia and latent feline leukaemia virus infection in cats with lymphoma. Journal of Feline Medicine and Surgery 13: 81–87.

Tailor CS, Willett BJ and Kabat D (1999) A putative cell surface receptor for anemia‐inducing feline leukemia virus subgroup C is a member of a transporter superfamily. Journal of Virology 73: 6500–6505.

Takeuchi Y, Vile RG, Simpson G et al. (1992) Feline leukemia virus subgroup B uses the same cell surface receptor as gibbon ape leukemia virus. Journal of Virology 66: 1219–1222.

Tsatsanis C, Fulton R, Nishigaki K et al. (1994) Genetic determinants of feline leukemia virus‐induced lymphoid tumors: patterns of proviral insertion and gene rearrangement. Journal of Virology 68: 8294–8303.

Further Reading

Hardy WD Jr (1993) Feline oncoretroviruses. In: Levy JA (ed.) The Retroviridae, vol. 2, pp. 109–120. New York: Plenum Press.

Onions DE and Neil JC (1994) Feline leukemia and sarcoma viruses. In: Webster RG and Granoff A (eds) Encyclopedia of Virology, vol. 1, pp. 459–463. London: Academic Press.

Rohn JL, Gwynn SR, Lauring AS, Linenberger ML and Overbaugh J (1996) Viral genetic variation, AIDS, and the multistep nature of carcinogenesis: the feline leukemia virus model. Leukemia 10: 1867–1869.

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Jarrett, Oswald, and Neil, James C(Apr 2012) Feline Leukaemia Virus. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001021.pub2]